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(Hypertension. 2007;50:463.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Lipids and the Heart

Neither Feast nor Famine

Denis J. Glenn; David G. Gardner

From the Diabetes Center and Department of Medicine, University of California at San Francisco.

Correspondence to Denis J. Glenn, 1119 HSW, Diabetes Center, University of California at San Francisco, San Francisco, CA 94143-0540. E-mail dglenn@diabetes.ucsf.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The role of serum lipids in cardiovascular disease risk is well established, and reduction of serum lipid levels is now a cornerstone in the treatment of coronary artery disease. Dysregulation of lipid metabolism is also thought to play a role in the development of heart failure, although the mechanisms behind this are incompletely understood.¹ Under normal conditions, the heart is primarily dependent on energy production derived from the ß-oxidation of fatty acids and, to a lesser extent, glycolysis. However, in heart failure, fatty acid use seems to be reduced.² The decrease in fatty acid oxidation and subsequent reduction in energy availability have been proposed to contribute to decreased contractile function of the heart. On the other hand, there is growing evidence that overaccumulation of fatty acid or triglyceride in the heart may be directly toxic to the myocyte, contributing to a process called cardiac lipotoxicity.¹

Because the heart depends on fatty acid oxidation for energy, the transport and storage of lipids in the myocyte are tightly regulated. Although precise quantification of lipid levels within the myocyte is technically difficult, triglyceride and free fatty acid levels are thought to be low under normal physiological conditions. As noted above, there is evidence to suggest that exaggerated accumulation of triglyceride or free fatty acid within the myocyte is linked to the development of cardiomyopathy (ie, cardiac lipotoxicity). In diabetic and obese patients with severe nonischemic heart failure, myocyte steatosis (ie, increased intramyocardial lipid accumulation) can be demonstrated.³ However, obesity and diabetes, as systemic . . . [Full Text of this Article]

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